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First published online March 20, 2009
doi: 10.1242/10.1242/dev.022418

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Chemokine signaling in embryonic cell migration: a fisheye view

Institute of Cell Biology, ZMBE, University of Münster, Von-Esmarch-Straße 56, 48149 Münster, Germany.

View larger version (75K): [in this window] [in a new window]   Fig. 1. Chemokines in zebrafish gastrulation. (A-C, top) Zebrafish embryos at 8 hours post-fertilisation (hpf), anterior to the top, labeled for expression of foxa2. Dotted lines represent the endodermal cell front. (Bottom) Schematic cross-section representing the mesoderm-endoderm interactions during gastrulation. In wild-type zebrafish embryos (A), chemokine signaling coordinates the migration of the endoderm with that of the mesoderm during gastrulation. The endodermal cell front of gastrulating zebrafish embryos is abnormally displaced in embryos in which CXCL12b (B) or CXCR4a (C) is knocked down, and integrin-based tethering between the endodermal and mesodermal germ layers, which depends on attachment to the extracellular matrix (ECM), is reduced. [Top panels adapted, with permission, from Nair and Schilling (Nair and Schilling, 2008)].

View larger version (42K): [in this window] [in a new window]   Fig. 2. Chemokines in individual cell migration. (A-D, top) Zebrafish embryos at 20-23 hpf, anterior to the top, with primordial germ cells (PGCs) expressing green fluorescent protein (GFP). (Bottom) Schematic representation of PGC target-tissue interactions during PGC migration. (A) In the wild-type, the directional migration of individual PGCs is controlled by chemokines. (B) In the absence of CXCL12a, no chemokine gradient is formed, and the PGCs fail to migrate towards their target. (C) Similarly, in the absence of the corresponding CXCR4b receptor, the cells fail to respond to the chemotactic gradient formed by CXCL12a. (D) Lower levels of CXCR7b, which usually sequesters CXCL12a, result in abnormally high levels of CXCL12a and in defects in PGC polarization and directional migration. [Top panel in B adapted, with permission, from Doitsidou et al. (Doitsidou et al., 2002)].

View larger version (46K): [in this window] [in a new window]   Fig. 3. Chemokines in collective cell migration in the zebrafish lateral line primordium. (A-D, top) Cldnb::lynGFP transgenic zebrafish embryos at 42 hpf, anterior to the left, with the posterior lateral line primordium (PLLP) labeled with GFP (arrowheads). (Bottom) Schematic representation of chemokine signaling in the collective migration of the PLLP. (A) In the wild-type, cells at the back of the PLLP (left) express CXCR7b (red dots), which sequesters CXCL12a (dark yellow), thereby generating a chemokine gradient over the migrating cluster. (B) In Cxcl12a-/- embryos, the PLLP cluster fails to polarize and does not move. (C) Similarly, in the PLLP clusters of Cxcr4b-/- embryos, the CXCL12a gradient is not interpreted by cells at the front of the cluster, and the PLLP does not migrate. (D) PLLP clusters in which CXCR7b is knocked down fail to generate the CXCL12a gradient and therefore do not migrate. [Fluorescence images adapted, with permission, from Valentin et al. (Valentin et al., 2007)].

View larger version (70K): [in this window] [in a new window]   Fig. 4. Chemokines in cell positioning in the mouse cerebellum. (A-C, top) Coronal sections of mouse embryonic day 18.5 cerebellar tissue stained with Hematoxylin and Eosin. Arrowheads indicate the external granule layer, asterisk indicates the Purkinje cell layer. (Bottom) Schematic representation of chemokine function in granule cell precursor localization in the developing mouse cerebellum. (A) In the wild-type, granule precursor cells are initially maintained at the external granule layer (upper domain of the box) of the cerebellum. (B,C) In Cxcl12-/- or Cxcr4-/- mice, granule precursor cells migrate prematurely into deeper layers of the cerebellum (lower regions in the boxes). [Top panels adapted, with permission, from Ma et al. (Ma et al., 1998)].

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